RESPIRATORY FAILURE

Respiratory • Respiratory disfunction clinically significant to

produce discomfort
Impairment
Respiratory • Respiratory disturbance, strong enough to hamper
certain daily activities, that can be measured from the
insufficiency mechanic of breathing and or from gas exchange

Respiratory • Increase and worsening respiratory effort that can be

seen from clinical appearance
distress
Respiratory • Disturbance of 1 (one) aspect or more respiratory
Failure function and life threatening
 INTRODUCTION
● Respiratory failure is a condition in which the respiratory system fails in
oxygenation or carbon dioxide elimination or both.
● There are 2 types of impaired gas exchange: (1) hypoxemic respiratory
failure, which is a result of lung failure, and (2) hypercapnic respiratory
failure, which is a result of respiratory pump failure

Vo P and Kharasch V,S., 2014. Respiratory failure. Ped in rev

 Type of Respiratory Failure
Type 1: Type 2:
Hypoxemic Hypercapnic
respiratory respiratory
failure failure
• Ventilation-perfusion (V/Q) PaCO2 ≥ 45 mmHg, PaO2 <
mismatch results in the 60 mmHg
decrease of PaO2) to below
60 mm Hg with normal or
low PaCO2
• In this type, the gas
exchange is impaired at the
level of alveoli-capillary
membrane.
• Examples of type I
respiratory failures are
carcinogenic or non-
cardiogenic
Vo P and Kharasch V,S., 2014. Respiratory failure. Pedpulmonary
in rev
edema and
Buku Ajar Pulmonologi dan Kedokteran Respirasi, severe
2018
 Type 1: Hypoxemic respiratory
failure

Figure 1. The pathophysiological mechanism

and clinical causes of hypoxaemic respiratory
failure

Suh, E.S. and Hart, N., 2012. Respiratory failure. Medicine, 40(6), pp.293-297.
 Type 2: Hypercapnic respiratory
failure

Figure 2. Hypercapnic respiratory failure arises

as a result of an imbalance between the three
components of the respiratory muscle pump:
the load on the respiratory system, the capacity
of the respiratory muscle pump and neural
respiratory drive

Suh, E.S. and Hart, N., 2012. Respiratory failure. Medicine, 40(6), pp.293-297.
 ETIOLOGY

Vo P and Kharasch V,S., 2014. Respiratory failure. Ped in rev

 ETIOLOGY
Respiratory Failure type I Respiratory Failure type II

Pneumonia Myasthenia Gravis

Pulmonary edema Tetanus

Pneumothorax Chronic Obstructive Pulmonary Disease

Asthma Cervical trauma and Head Trauma

Pulmonary Embolism Pulmonary Edema

Artery Pulmonary Hypertension Severe Asthma

Pneumoconiosis Acute Respiratory Distress Syndrome

Acute Respiratory Distress Syndrome

Buku Ajar Pulmonologi dan Kedokteran Respirasi, 2018

 SIGN AND
SYMPTOMS

Vo P and Kharasch V,S., 2014. Respiratory failure. Ped in rev

 EVALUATION
Arterial Blood Gas
• The information obtained from an ABG includes pH, partial pressure of arterial
oxygen (PaO2), partial pressure of arterial carbon dioxide (PaCO2), and serum
bicarbonate (HCO3)
Chest X-Ray
• To help identify or confirm the cause of the respiratory failure

Another cause of respiratory failure

• Complete blood count (CBC)
• Sputum, blood and urine culture
• Blood electrolytes and thyroid function tests
• Pulmonary function tests
• Electrocardiography (ECG)
• Echocardiography
• Bronchoscopy

Shebl, E. and Burns, B., 2018. Respiratory failure.

 Interpretation of Blood Gas

Vo P and Kharasch V,S., 2014. Respiratory failure. Ped in rev

 MANAGEMENT
Correction of Hypoxemia
• The goal is to maintain adequate tissue oxygenation, generally
achieved with an arterial oxygen tension (PaO2) of 60 mm Hg or
arterial oxygen saturation (SaO2), about 90%
Correction of Hypercapnia and Respiratory Acidosis
• This may be achieved by treating the underlying cause or providing
ventilatory support
Ventilatory Support
• The goals of ventilatory support in respiratory failure are to correct
hypoxemia, correct acute respiratory acidosis and resting of ventilatory
muscle

Shebl, E. and Burns, B., 2018. Respiratory failure.

 MANAGEMENT
● Treatment of respiratory failure should be directed towards the underlying cause while
providing support with oxygenation and ventilation, if necessary.

● The treatment includes supportive measures and treatment of the underlying cause.
However, the initial steps in managing patients with acute respiratory failure should start by
assessing the airway, breathing, and circulation (ABC).

● If the patient is not alert and responsive then simple measures to maximize airway patency
e such as a jaw thrust maneuver or use of an oropharyngeal airway should be performed
and an anesthetist called immediately to assist.

● Supportive measures depend on patent airways to maintain adequate oxygenation,

ventilation, and correction of blood gas abnormalities.

● It is also appropriate to ask for early assistance from outreach teams or inform the high-
dependency unit (HDU) or intensive care unit (ICU) as ongoing management may need to
be continued in one of these settings.

● It is important to stress that high-flow oxygen therapy should always be given to a patient
who is hypoxic.

Vo P and Kharasch V,S., 2014. Respiratory failure. Ped in rev

Burt, C.C. and Arrowsmith, J.E., 2009. Respiratory failure. Surgery (Oxford), 27(11), pp.475-479.
 Escalation therapeutic strategy, integrative supports and
management of acute respiratory failure

Scala, R. and Heunks, L., 2018. Highlights in acute respiratory failure.

 MECHANICAL VENTILATION
INDICATION
● Apnea with respiratory arrest
● Tachypnea with respiratory rate >30 breaths per minute
● Disturbed conscious level or coma
● Respiratory muscle fatigue
● Hemodynamic instability
● Failure of supplemental oxygen to increase PaO2 to 55 to 60
mmHg
● Hypercapnea with arterial pH less than 7.25

The goal of mechanical ventilation is to relieve

respiratory distress by decreasing the inspiratory work
of breathing, improving pulmonary gas exchange,
allowing the lungs to heal, reversing respiratory muscle
fatigue, and preventing further complications due to
abnormal gas exchange
Shebl, E. and Burns, B., 2018. Respiratory failure.
 DIFFERENTIAL DIAGNOSIS
● Cardiogenic shock
● Cor pulmonale
● Diaphragmatic Paralysis
● Dilated Cardiomyopathy
● Myocardial Infarction
● Obstructive shock
● Obstructive sleep apnea
● Pulmonary Embolism
● Pulmonary arterial hypertension

Shebl, E. and Burns, B., 2018. Respiratory failure.

 COMPLICATION
● Respiratory failure is associated with both pulmonary and
extrapulmonary complications, especially in the acute
setting.
● Pulmonary complications include bronchopleural fistula,
nosocomial pneumonia, pneumothorax, pulmonary
embolism, and pulmonary fibrosis,
● While extrapulmonary complications include acid-base
disturbances, decreased cardiac output, gastrointestinal
hemorrhage, hepatic failure, ileus, infection, increased
intracranial pressure, malnutrition, pneumoperitoneum, renal
failure, and thrombocytopenia

Shebl, E. and Burns, B., 2018. Respiratory failure.

References
1. Shebl, E. and Burns, B., 2018. Respiratory failure.
2. Burt, C.C. and Arrowsmith, J.E., 2009. Respiratory failure. Surgery
(Oxford), 27(11), pp.475-479.
3. Vo P and Kharasch V,S., 2014. Respiratory failure. Ped in rev
4. Suh, E.S. and Hart, N., 2012. Respiratory failure. Medicine, 40(6), pp.293-297.
5. Scala, R. and Heunks, L., 2018. Highlights in acute respiratory failure.
6. Buku Ajar Pulmonologi dan Kedokteran Respirasi, 2018
ARDS
Definisi
● ARDS merupakan sindrom yang ditandai oleh peningkatan permeabilitas membran
alveolar-kapiler terhadap air, larutan protein plasma, disertai kerusakan alveolar difus
dan akumulasi cairan dalam parenkim paru.
● Gagal nafas akut
● Radiografi dada : infiltrat alveolar bilateral tanpa adanya bukti edema paru kardiogenik
● PaO2 / FiO2 < 200 mmHg
● PaO2 / FiO2 200- 300 mmHg  Acute Lung Injury
Etiologi

Fishman's Pulmonary Diseases and Disorders ,

2019
● Cari : Kriteria Berlin untuk ARDS
Patofisiologi

Diagram yang mengilustrasikan perjalanan waktu untuk pengembangan dan penyelesaian

ARDS
●Fase eksudatif (7 hari awal) setelah paparan

•Insult kerusakan endotel kapiler alveolus & pneumosit tipe I  kerusakan barrier/tight junction alveolus  edema
alveolar & interstistial (cairan+protein)
•Insult aktivasi makrofagsitokin proinflamasi (IL-1, IL8, TNF a, Leukotrien)rekrutmen leukosit (neutrofil-monosit)
mediator toksik kerusakan   edema alveolus(cairan+protein) disfungsi surfaktanmembrane hialin)plasma
protein+debris sel+surfaktan abnormal)kolaps alveolus

•Sitokin pro inflamasi pulmonary vascular injuryagregasi platelet+mikrotrombus

Harrison, ers handbook of Respiratory Medicine, 2021

●Fase proliferative (7-21 hari)
•Perbaikan gejala
•Shift sel inflamasi dari neutrofillimfosit

•Inisiasi repair sel alveolar tipe II bereplikasi menjadi sel tipe I, organisasi eksudat
Fase Fibrosis
● Proliferasi & migrasi fibroblast ke alveolar dan interstistium proses fibrosis, distorsi asinar emfisema, fibrosis
intima vascular paru PH
Gejala Klinis
• Sindrom ini ditandai dengan dispnea dan hipoksemia
• Semakin memburuk dalam waktu 6 hingga 72 jam
• Anamnesis untuk mengidentifikasi Etiologi.
• Pasien sering mengeluhkan sesak napas ringan pada
awalnya, memberat dalam waktu 12 Jam sampai 1 hari.
• Menjadi parah dan membutuhkan ventilasi mekanis
untuk mencegah hipoksia.
Diagnosis
• onset akut
●umumnya 3-5 hari sejak adanya diagnosis kondisi yang menjadi faktor risiko ARDS
●infiltrat paru bilateral pada radiografi dada yang bukan berasal dari jantung
●Rasio PaO2/FiO2 kurang dari 200 mmHg
Pemeriksaan Penunjang
●Laboratorium AGD : Alkalosis respiratorik pada fase awal, dan berganti menjadi asidosis
respiratorik pada fase lanjut
●Leukositosis (sepsis), anemia, trombositopenia (SIRS), peningkatan kadar amilase (pankreatitis)
●Gangguan fungsi ginjal dan hati.
●PencitraanFoto dada : gambaran radioopak difus
●CT-Scan : pola heterogen, predominasi infiltrat pada dorsal paru (supine)
●Alkalosis respiratorik : elevated arterial blood pH, low PCO2
●Acidosis respiratorik : decrease arterial blood pH, high PCO2
CXR : kekeruhan alveolar
dan interstisial
melibatkan setidaknya
tiga perempat lapangan
paru, dan dapat
dibedakan dari edema
paru kardiogenik

ARDS Jarang
menunjukkan
kardiomegali, efusi
pleura, atau redistribusi
 CT scan thorax
representatif selama
fase eksudatif ARDS

edema alveolar dependen

dan atelektasis
mendominasi.

CT Thorax :
menunjukkan luas
heterogenitas paru
Penatalaksanaan
● Strategi perawatan utama adalah perawatan suportif dan berfokus pada
● 1) mengurangi fraksi shunt,
● 2) meningkatkan pengiriman oksigen,
● 3) mengurangi konsumsi oksigen, dan
● 4) menghindari cedera lebih lanjut.
Penatalaksanaan
●Ambil alih fungsi pernapasan dengan ventilator mekanik
Obat-obatan : Terapi penyebab dasar terjadinya ARDS
●Kortikosteroid Inhalasi
●Nitric Oksida (NO)
●Diuretik
●Sedativa, analgetik dan antipiretik
●Posisi pasien : telungkup meningkatkan oksigenasi tetapi tidak mengubah mortalitas
●Mengatur keseimbangan cairan : mempertahankan perfusi adekuat tanpa mengorbankan
oksigenasi
Komplikasi
● Komplikasi Multiorgan dysfunction syndrome (MODS) Pneumonia nosocomial
●
Barotrauma, pneumotoraks
● Trauma laring
● Trakeomalasia
● Fistula trakeo-esofageal
● Kematian
Prognosis
●Prognosis Mortalitas sekitar 40% & 90% jika disertai sepsis

●Prognosis dipengaruhi oleh :

●Penyakit dasar Adanya keganasan
●Adanya atau timbulnya disfungsi organ multiple
●Usia
●Ada atau tidaknya perbaikan dalam indeks pertukaran gas, seperti rasio PaO2/FiO2 dalam 3-7
hari pertama.
●Pasien yang membaik akan mengalami pemulihan fungsi paru dalam 3 bulan dan mencapai
fungsi maksimum yang dapat dicapai pada bulan keenam setelah ekstubasi.
●50% pasien akan tetap memiliki abnormalitas, termasuk gangguan restriksi dan penurunan
kapasitas difusi. Juga terjadi penurunan kualitas hidup.
THANK
YOU